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| Title: | N-acetylcysteineamide (NACA) prevents inflammation and oxidative stress in animals exposed to diesel engine exhaust |
| Author (s): | Banerjee, Atrayee Trueblood, Max B. Zhang, Xinsheng Manda, Kalyan Reddy Lobo, Prem Whitefield, Philip D. Hagen, Donald Edward Ercal, Nuran |
| Department/Lab Affiliations: | Center for Environmental Science and Technology (CEST) Chemistry Environmental Research Center Mechanical & Aerospace Engineering Physics |
| Subject Terms: | Air - pollution Antioxidants. Lungs. |
| Issue Date: | 2009-06 |
| Publisher: | Elsevier |
| Citation: | Banerjee, Atrayee, Max B. Trueblood, Xinsheng Zhang, Kalyan Reddy Manda, Prem Lobo, Philip D. Whitefield, Donald E. Hagen and Nuran Ercal. "N-acetylcysteineamide (NACA) prevents inflammation and oxidative stress in animals exposed to diesel engine exhaust," Toxicology Letters, Volume 187, Issue 3, (June 2009):187-193. |
| Abstract: | Diesel exhaust particles (DEPs), a by-product of diesel engine exhaust (DEE), are one of the major components of air borne particulate matter (PM) in the urban environment. DEPs are composed of soot, polycyclic aromatic hydrocarbons (PAHs), redox active semi-quinones, and transition metals, which are known to produce pro-oxidative and pro-inflammatory effects, thereby leading to oxidative stress-induced damage in the lungs. The objective of this study was to determine if N-acetylcysteineamide (NACA), a novel thiol antioxidant, confers protection to animals exposed to DEPs from oxidative stress-induced damage to the lung. To study this, male C57BL/6 mice, pretreated with either NACA (250 mg/kg body weight) or saline, were exposed to DEPs (15 mg/m3) or filtered air (1.5–3 h/day) for nine consecutive days. The animals were sacrificed 24 h after the last exposure. NACA-treated animals exposed to DEP had significant decreases in the number of macrophages and the amount of mucus plug formation in the lungs, as compared to the DEP-only exposed animals. In addition, DEP-exposed animals, pretreated with NACA, also experienced significantly lower oxidative stress than the untreated group, as indicated by the glutathione (GSH), and malondialdehyde (MDA) levels and catalase (CAT) activity. Further, DEP-induced toxicity in the lungs was reversed in NACA-treated animals, as indicated by the lactate dehydrogenase levels. Taken together, these data suggest that the thiol-antioxidant, NACA, can protect the lungs from DEP-induced inflammation and oxidative stress related damage. |
| Type: | Article - Journal text |
| In Title: | Toxicology Letters |
| Copyright Notice: | This material is presented to ensure timely dissemination of scholarly and technical work. Copyright and all rights therein are retained by authors or by other copyright holders. All persons copying this information are expected to adhere to the terms and constraints invoked by each author's copyright. In most cases, these works may not be reposted without the explicit permission of the copyright holder. Pre-print: author can archive; Post-print: author can archive; FULL COPYRIGHT INFORMATION: |
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| title | N-acetylcysteineamide (NACA) prevents inflammation and oxidative stress in animals exposed to diesel engine exhaust |
| contributor.author | Banerjee, Atrayee |
| contributor.author | Trueblood, Max B. |
| contributor.author | Zhang, Xinsheng |
| contributor.author | Manda, Kalyan Reddy |
| contributor.author | Lobo, Prem |
| contributor.author | Whitefield, Philip D. |
| contributor.author | Hagen, Donald Edward |
| contributor.author | Ercal, Nuran |
| contributor.deptlab | Center for Environmental Science and Technology (CEST) |
| contributor.deptlab | Chemistry |
| contributor.deptlab | Environmental Research Center |
| contributor.deptlab | Mechanical & Aerospace Engineering |
| contributor.deptlab | Physics |
| contributor.sponsor | National Institute of Health |
| subject.LCSH | Air - pollution |
| subject.LCSH | Antioxidants. |
| subject.LCSH | Lungs. |
| date.issued | 2009-06 |
| publisher | Elsevier |
| identifier.citation | Banerjee, Atrayee, Max B. Trueblood, Xinsheng Zhang, Kalyan Reddy Manda, Prem Lobo, Philip D. Whitefield, Donald E. Hagen and Nuran Ercal. "N-acetylcysteineamide (NACA) prevents inflammation and oxidative stress in animals exposed to diesel engine exhaust," Toxicology Letters, Volume 187, Issue 3, (June 2009):187-193. |
| identifier.pub.URI | |
| description.abstract | Diesel exhaust particles (DEPs), a by-product of diesel engine exhaust (DEE), are one of the major components of air borne particulate matter (PM) in the urban environment. DEPs are composed of soot, polycyclic aromatic hydrocarbons (PAHs), redox active semi-quinones, and transition metals, which are known to produce pro-oxidative and pro-inflammatory effects, thereby leading to oxidative stress-induced damage in the lungs. The objective of this study was to determine if N-acetylcysteineamide (NACA), a novel thiol antioxidant, confers protection to animals exposed to DEPs from oxidative stress-induced damage to the lung. To study this, male C57BL/6 mice, pretreated with either NACA (250 mg/kg body weight) or saline, were exposed to DEPs (15 mg/m3) or filtered air (1.5–3 h/day) for nine consecutive days. The animals were sacrificed 24 h after the last exposure. NACA-treated animals exposed to DEP had significant decreases in the number of macrophages and the amount of mucus plug formation in the lungs, as compared to the DEP-only exposed animals. In addition, DEP-exposed animals, pretreated with NACA, also experienced significantly lower oxidative stress than the untreated group, as indicated by the glutathione (GSH), and malondialdehyde (MDA) levels and catalase (CAT) activity. Further, DEP-induced toxicity in the lungs was reversed in NACA-treated animals, as indicated by the lactate dehydrogenase levels. Taken together, these data suggest that the thiol-antioxidant, NACA, can protect the lungs from DEP-induced inflammation and oxidative stress related damage. |
| type | Article - Journal |
| type.DCMIType | text |
| type.status | Postprint |
| relation.isPartOf | Toxicology Letters |
| rights | This material is presented to ensure timely dissemination of scholarly and technical work. Copyright and all rights therein are retained by authors or by other copyright holders. All persons copying this information are expected to adhere to the terms and constraints invoked by each author's copyright. In most cases, these works may not be reposted without the explicit permission of the copyright holder. |
| rights | Pre-print: author can archive; Post-print: author can archive; |
| rights.URI | |
| identifier.persist.URI | |
| date.available | 2009-05-20T20:55:52Z |